Mitochondrial reactive oxygen species and cancer
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2049-3002-2-17.pdf
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813.86 KB
Format
Adobe PDF
Checksum (MD5)
67d46bb174c5cd44c8241a057ecce7c2
Author(s)
Chandel, Navdeep S
Sullivan, Lucas Bryan
Date Issued
November 2014
Journal
Cancer & Metabolism
Publisher
BioMed Central Ltd
Citation
Sullivan, Lucas B, and Navdeep S Chandel. “Mitochondrial Reactive Oxygen Species and Cancer.” Cancer & Metabolism 2.1 (2014): 17.
Version
Final published version
Abstract
Mitochondria produce reactive oxygen species (mROS) as a natural by-product of electron transport chain activity. While initial studies focused on the damaging effects of reactive oxygen species, a recent paradigm shift has shown that mROS can act as signaling molecules to activate pro-growth responses. Cancer cells have long been observed to have increased production of ROS relative to normal cells, although the implications of this increase were not always clear. This is especially interesting considering cancer cells often also induce expression of antioxidant proteins. Here, we discuss how cancer-associated mutations and microenvironments can increase production of mROS, which can lead to activation of tumorigenic signaling and metabolic reprogramming. This tumorigenic signaling also increases expression of antioxidant proteins to balance the high production of ROS to maintain redox homeostasis. We also discuss how cancer-specific modifications to ROS and antioxidants may be targeted for therapy.
MIT Department
Koch Institute for Integrative Cancer Research at MIT
Terms of Use
Creative Commons Attribution
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1186/2049-3002-2-17
